Results: All animals presented delayed motor neuron death. The number of intact neurons decreased correlatively with neurologic function. No obvious terminal deoxynucleotidyl transferase-mediated deoxyuridine

triphosphatebiotin nick-end labeling-positive cells were observed. Glial fibrillary acidic protein expression increased with time in both the gray and white matter, representing the development of reactive astrogliosis. Significant correlation was found between glial fibrillary acidic protein expression and the number of intact motor neurons on the third day in both the gray (r(2) = 0.726, P = .031) and white (r(2) = 0.927, P = .002) matter.

Conclusions:

Reactive astrogliosis 3 days after transient spinal cord ischemia correlates with the number of intact motor neurons. Our method for semiquantitative Citarinostat datasheet DMXAA analysis of reactive astrogliosis is simple and reproducible and seems useful for such experimental studies.”
“The contribution of vasodilator cyclooxygenase (COX) metabolites to the maintenance of the cerebrocortical blood flow (CBF) has been studied under physiological conditions and in nitric oxide (NO) deficiency. Inhibition of COX decreased resting CBF without changing arterial blood pressure. NO synthase blockade resulted in hypertension and CBF reduction as well as in enhanced cerebral prostacyclin and prostaglandin E(2) production. Despite the increased vasodilator prostanoid release in the absence of NO, the CBF-decreasing effect of COX blockade failed to increase. Therefore, the COX pathway seems to play a similar role under physiological and NO-deficient conditions in the maintenance of the resting CBF NeuroReport 20:1027-1031 (C) 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.”
“Objective:

Cyclophosphamide has a role of decreasing high-sensitivity C-reactive protein enough in the treatment of autoimmune disorders. The effect of cyclophosphasmide on high-sensitivity C-reactive protein was investigated in myocardial ischemia/reperfusion rat.

Methods: Open-chest rats were submitted to 30 minutes of ischemia and followed for 3, 12, or 24 hours of reperfusion. All 72 rats survived and were divided into sham, ischemia/reperfusion (I/R) and cyclophosphamide groups, and each group included 3 time-point subgroups (3, 12, and 24 hours; n = 8 for each subgroup). Cyclophosphamide (0.75 g/m(2)) or saline was intraperitoneally administrated in the cyclophosphamide or I/R group. A polyethylene tube was inserted into the left ventricular cavity to detect left ventricular systolic pressure, left ventricular end-diastolic pressure, and maximum rate of rise or fall of left ventricular pressure.